The aim of the present work was to study the dynamics of presynaptic modification in conditions of blockade of GABA receptor NR2B subunits, which are key for consolidation of LTP. This was addressed by studying the developmental features of NMDA-dependent long-term potentiation (LTP) in field CA1 of living rat hippocampal slices incubated with ifenprodil by testing with paired-pulse stimuli throughout the recording period before and for 1 h after high-frequency stimulation of Schaffer collaterals (100 Hz, 1 sec). Perfusion of slices with ifenprodil had no effect on the baseline characteristics of CA3–CA1 synapses in terms of the relationship between the amplitudes of the first and second responses and stimulus intensity, i.e., paired-pulse facilitation. LTP was signifi cantly less marke d in slices incubated with ifenprodil, while potentiation of the second response in the pair was essentially the same in the control and experimental groups. In control slices, potentiation was accompanied by a significant decrease in PPF immediately after tetanization. This effect was not seen in slices incubated with ifenprodil; furthermore, a transient increase in PPF was seen 15 min after tetanization. In both groups, early LTP was increased proportionately to the decrease in PPF. In the absence of presynaptic modifications, LTP was weakened, including in control slices, and an increase in PPF in experimental slices was accompanied by temporary depression of focal potentials. Ifenprodil had no obvious effect on the maintenance of LTP. It is suggested that detection of the adverse influence of ifenprodil on the process of consolidation requires complex analysis taking account of all the factors operating. The results obtained here support a tight link between LTP and modification s of pairedpulse plasticity and provide grounds for suggesting that NMDA receptor NR2B subunits are directly related to the involvement of the presynaptic component in long-term synaptic potentiation.
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